Can prediabetes be “cured”? In the early stages of prediabetes (and type 2 diabetes), diligent attention to food choices and activity, and most importantly weight loss, can improve blood sugar numbers, effectively “reversing” the disease and reducing the odds of developing type 2 diabetes. However, some people may have underlying factors (such as family history and genetics) that put them at a greater risk of type 2 diabetes, meaning they will always require careful attention to blood sugar levels and lifestyle choices. Returning to old habits will likely put someone back on the road to prediabetes, and eventually, type 2 diabetes.
Grains: Grains, especially gluten-containing grains like wheat, contain large amounts of carbohydrates that are broken down into sugar within only a few minutes of consumption. Gluten can cause intestinal inflammation, which affects hormones like cortisol and leptin, and can lead to spikes in blood sugar. I recommend removing all grains from your diet for 90 days as your body adjusts to this healing program. Then you can try bringing sprouted ancient grains back into your diet in small amounts.
The reason the body stops producing insulin is that it kills off the pancreas’ beta cells, which produce insulin. People with Type 1 diabetes must get their insulin from injections or ingestion, a cumbersome and often imprecise task. Too little insulin and blood sugar levels stay high for extended periods, potentially damaging the body; too much and blood sugar levels crash, possibly causing a person with diabetes to faint or experience an even worse problems, such as a stroke.
Cinnamonium cassia and its relative C. burmanii are the types of cinnamon that have the best effect on diabetes symptoms. There have been numerous studies on cinnamon and, overall, they have shown cinnamon can slow stomach emptying and lower postprandial glucose levels. It also reduces glucose levels in Type 2 Diabetes Mellitus patients who have had poor diabetic control. It may also be helpful in lowering insulin levels, blood pressure, and A1C, and reduce AGE formation. This is a safe herb for diabetics. A good dose is 1 to 2 g a day or 200 mg or more of a concentrated extract.
Khodneva, Y., Shalev, A., Frank, S. J., Carson, A. P., & Safford, M. M. (2016, May). Calcium channel blocker use is associated with lower fasting serum glucose among adults with diabetes from the REGARDS study. Diabetes Research and Clinical Practice, 115, 115-121. Retrieved from http://www.diabetesresearchclinicalpractice.com/article/S0168-8227(16)00070-X/abstract
Rosiglitazone (Avandia) and pioglitazone (ACTOS) are in a group of drugs called thiazolidinediones. These drugs help insulin work better in the muscle and fat and also reduce glucose production in the liver. The first drug in this group, troglitazone (Rezulin), was removed from the market because it caused serious liver problems in a small number of people. So far rosiglitazone and pioglitazone have not shown the same problems, but users are still monitored closely for liver problems as a precaution. Both drugs appear to increase the risk for heart failure in some individuals, and there is debate about whether rosiglitazone may contribute to an increased risk for heart attacks. Both drugs are effective at reducing A1C and generally have few side effects.
Clearly separate from the characteristic lack of acute insulin secretion in response to increase in glucose supply is the matter of total mass of β-cells. The former determines the immediate metabolic response to eating, whereas the latter places a long-term limitation on total possible insulin response. Histological studies of the pancreas in type 2 diabetes consistently show an ∼50% reduction in number of β-cells compared with normal subjects (66). β-Cell loss appears to increase as duration of diabetes increases (67). The process is likely to be regulated by apoptosis, a mechanism known to be increased by chronic exposure to increased fatty acid metabolites (68). Ceramides, which are synthesized directly from fatty acids, are likely mediators of the lipid effects on apoptosis (10,69). In light of new knowledge about β-cell apoptosis and rates of turnover during adult life, it is conceivable that removal of adverse factors could result in restoration of normal β-cell number, even late in the disease (66,70). Plasticity of lineage and transdifferentiation of human adult β-cells could also be relevant, and the evidence for this has recently been reviewed (71). β-Cell number following reversal of type 2 diabetes remains to be examined, but overall, it is clear that at least a critical mass of β-cells is not permanently damaged but merely metabolically inhibited.
Although the promises are big, these technologies are still far from the market. First, clinical trials will have to show they do work. Then, the price could be steep, as cell therapy precedents for other applications, such as oncology, come with price tags that reach the six figures and are finding difficulties to get reimbursed. Considering that compared to cancer, diabetes is not an immediately life-threatening disease, health insurers in some countries might be reluctant to cover the treatment.
Whole-body insulin resistance is the earliest predictor of type 2 diabetes onset, and this mainly reflects muscle insulin resistance (26). However, careful separation of the contributions of muscle and liver have shown that early improvement in control of fasting plasma glucose level is associated only with improvement in liver insulin sensitivity (20,21). It is clear that the resumption of normal or near-normal diurnal blood glucose control does not require improvement in muscle insulin sensitivity. Although this finding may at first appear surprising, it is supported by a wide range of earlier observations. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (27). Humans who have the PPP1R3A genetic variant of muscle glycogen synthase cannot store glycogen in muscle after meals but are not necessarily hyperglycemic (28). Many normoglycemic individuals maintain normal blood glucose levels with a degree of muscle insulin resistance identical to those with type 2 diabetes (29).
The researchers have cured mice, which are genetically similar to people but different enough that new rounds of animal testing — and millions of dollars more — are needed before human trials can begin. The researchers’ approach is sure to garner skeptics, at least in part because it is a significant departure from the many other attempts at curing diabetes, which typically involve transplanting new cells and/or suppressing the immune system’s attempts to kill off useful ones.
In adults, a rare side effect of taking diabetes pills is lactic acidosis, a very serious condition caused by a buildup of lactic acid in the blood. Lactic acidosis can cause symptoms like rapid breathing, muscle pain, cool and clammy skin, sweet-smelling breath, nausea, and vomiting. This problem has mostly happened in elderly people who have other medical problems in addition to their diabetes.
I bring this up because sleep apnea increases a person’s risk for developing type 2 diabetes. Also, sleep-disordered breathing is also related to proper nutrition throughout life. And perhaps most importantly, the first line of defense in catching sleep-disordered breathing in patients early, are dentists. This is another area where dentists must get involved if we want to tackle the issue of pervasive type 2 diabetes with any success.